Age-Related Changes in Renal Cyclic Nucleotides and Eicosanoids in Response to Sodium Intake
Author(s) -
Lesley J. Millatt,
Helmy M. Siragy
Publication year - 2000
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.35.2.643
Subject(s) - endocrinology , medicine , sodium , prostaglandin e , prostaglandin e2 , prostaglandin , kidney , low sodium , low sodium diet , chemistry , renin–angiotensin system , blood pressure , organic chemistry
The signaling molecules cGMP, cAMP, prostaglandin E(2) (PGE(2)), and prostaglandin F(2alpha) (PGF(2alpha)) play important roles in mediating the response of the kidney to changes in dietary sodium intake. We used a renal microdialysis technique in conscious rats to address the hypothesis that the renal ability to produce these mediators in response to dietary sodium intake is altered during maturation. Young (4-week-old) or adult (6-month-old) rats were studied after the consumption for 5 days of diets containing low (0. 04% NaCl), normal (0.28% NaCl), or high (4.0% NaCl) levels of sodium. Plasma renin activity was significantly increased by low-sodium diet and significantly decreased by high-sodium diet, with no significant difference between the responses of the 2 age groups. Renal interstitial fluid (RIF) levels of cGMP, cAMP, PGE(2), and PGF(2alpha) on normal-sodium diet were similar in the 2 age groups. Low-sodium diet caused a significant increase in RIF levels of all 4 mediators, with no significant differences between the responses of the 2 age groups. High-sodium diet also caused a significant increase in RIF levels of all 4 mediators. However, RIF production of cGMP, cAMP, and PGE(2) was significantly greater, and RIF PGF(2alpha) production was significantly lower, in young rats compared with adult rats. These data demonstrate that the kidneys of young and adult rats respond to dietary sodium restriction in a similar manner but that there are age-related changes in the renal response to sodium loading.
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